There are a number of procedural errors in this study which will be addressed as follows. Firstly the bias or affiliation of the study, published by Oxford University, is listed as pfizer, a corporation that makes smoking substitution products, and was caught bribing academics (in unlisted affiliations) with the intent of maintaining marijuana prohibition. Furthermore, the study was conducted in New Mexico, a part of the USA with high atmospheric radiation at this time, the non-smoking control received filtered air, while smoking groups were exposed to non-filtered air. The study asserts that in mice testing, supporting data was gathered that cigarettes cause pulmonary damage. The mice are divided into a control group, a “low-smoking” and a “high-smoking” group. The low-smoking group was exposed to the equivalent of between 20-30 cigarettes smoked continuously for six hours without stopping. The high-smoking group was exposed to the equivalent of 60 cigarettes per day continuously over a period of six hours and should have been disregarded as non-evident of human consumption patterns at any time in history. For the purposes of reality, the low-smokers (which in humans is at levels classified as heavy cigarette use), will be used in this evaluation. In addition, in this study the high smoking rats were starved (food consumption 60% of non-smokers), which also indicates this data is not reliable.Despite the conclusion and abstract’s assertion, the data is actually quite positive for regular smokers. Incidence rates of neoplasia in the nasal cavity was lower for smokers than non-smokers. The survival rate for smoking rats is higher by a significant amount, from 752 days to 779 days. Lung weight of smoking rats was the same as non-smoking rats (an increase was seen by 60 cigarettes per day). Ciliated cuboidal cell metaplasia (mucus in the lungs, a deformity frequently observed with aging that has not been definitively connected to cancer, except in epidermal cases, and then only correlatively) was noted in a small amount in smoking rats. Squamous metaplasia was not observed in smoking rats, but were noted in the 60 cigarette per day group. Keratinizing squamous cysts were not observed in smoking rats, but were noted rarely at 60 cigarettes per day. There were no consistent trends in lung lesions, with sometimes lowest levels in the group smoking 60 cigarettes per day (eg. hyperplasia), sometimes lower in smoking rats (eg. malignant neoplasia) and other times in non-smoking (eg. benign neoplasia), though it should be noted this occurred in non-significant levels in all rats. There is no increase in nasal neoplasia for smoking rats. After all this, the study asserts that cigarettes are the cause of problems, but admits, “The reason this study produced significant increases in lung tumors in rats while previous studies did not cannot be determined with certainty.” It is fairly clear that while, previous studies have linked regular human consumption to health benefits, the concept of gassing rats with 60 cigarettes per day had simply not occurred. See previous articles for data on cancer mortality rates in the USA and the probability that tobacco use in humans has numerous health benefits. While there is not data here on radiation exposure necessary to lower white blood cells in a rat, it is safe to assume these fall along similar lines with humans, and exposure to an unmeasured number of mrems of radiation was a significant factor in the development of malignancies in the rats. It is possible that filtered air might make a difference in mucous accumulation in rats as well as humans, though this is not definitively connected with cancer or malignant symptoms.